Galanin receptors modulate cutaneous vasodilation elicited by whole-body and local heating but not thermal sweating in young adults

Abstract

Galanin receptor subtypes GAL₁, GAL₂, and GAL₃ are involved in several biological functions. We hypothesized that 1) GAL₃ receptor activation contributes to sweating but limits cutaneous vasodilation induced by whole-body and local heating without a contribution of GAL₂; and 2) GAL₁ receptor activation attenuates both sweating and cutaneous vasodilation during whole-body heating. Young adults underwent whole-body (n = 12, 6 females) and local (n = 10, 4 females) heating. Forearm sweat rate (ventilated capsule) and cutaneous vascular conductance (CVC; ratio of laser-Doppler blood flow to mean arterial pressure) were assessed during whole-body heating (water-perfusion suit circulated with warm (35 °C) water), while CVC was also assessed by local forearm heating (from 33 °C to 39 °C and elevated to 42 °C thereafter; each level of heating maintained for ∼30 min). Sweat rate and CVC were evaluated at four intradermal microdialysis forearm sites treated with either 1) 5% dimethyl sulfoxide (control), 2) M40, a non-selective GAL₁ and GAL₂ receptor antagonist, 3) M871 to selectively antagonize GAL₂ receptor, or 4) SNAP398299 to selectively antagonize GAL₃ receptor. Sweating was not modulated by any GAL receptor antagonist (P > 0.169), whereas only M40 reduced CVC (P ≤ 0.003) relative to control during whole-body heating. Relative to control, SNAP398299 augmented the initial and sustained increase in CVC during local heating to 39 °C, and the transient increase at 42 °C (P ≤ 0.028). We confirmed that while none of the galanin receptors modulate sweating during whole-body heating, GAL₁ receptors mediate cutaneous vasodilation. Further, GAL₃ receptors blunt cutaneous vasodilation during local heating.

Keywords: Endothelium-dependent vasodilation; Neuropeptide; Thermoregulation.